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72 Cards in this Set

  • Front
  • Back
TOUCH Prescribing Program associated with Natalizumab (Tysabri)
1. prescribers and patients enrolled can prescribe and receive
2. certain pharmacies and infusion sites authorized can dispense and infuse
3. must re-authorize treatment every 6 months
Mechanism of Action of Mitoxantrone (Novantrone)
*IMMUNOSUPPRESSANT*
1. inhibits the proliferation of T-cells, B-cells, and macrophages; impairs the secretion of molecules that promote inflammation
Clinical Use of Mitoxantrone (Novantrone)
rapidly advancing MS disease who have failed other therapies
Major Contraindication for Mitoxantrone (Novantrone)
Cardiac Toxicity which can lead to CHF - must limit the amount per lifetime
Patient Education for Mitoxantrone (Novantrone)
1. Monitor for heart failure symptoms
2. monitor for symptoms of myelosuppression
3. blue-green urine color and bluish discoloration of sclera
Monitoring for Mitoxantrone (Novantrone)
1. Weight
2. LVEF (left ventricular ejection fraction)
3. CBC
4. LFTs
5. pregnancy test
Mechanism of Action of Fingolimod (Gilenya)
reduction of lymphocyte migration into the CNS
Clinical use of Fingolimod (Gilenya)
relapsing forms of MS; use as first or second-line therapy
Pregnancy Category for Fingolimod (Gilenya)
C - must use contraception during and for 2 months after stopping treatment
Monitoring for Fingolimod (Gilenya)
1. Bradycardia - electrocardiogram
2. Infections - CBC
3. Macular Edema - eye exams
4. Respiratory Effects - spirometric evaluation
5. Hepatic Effects - LFTs
Positive Lifestyle and Psychosocial for MS
1. very low saturated and vit D supplementation
2. minimal, regular sunlight exposure
3. positive mental and social health and coping
4. exercise
Risk Factors for Parkinson's
1. 1st degree relative
2. rural living
3. drinking well water
4. heavy metal, hydrocarbon, pesticide exposure
5. male
Pathophysiology of Parkinson's
* Dopamine stores are depleted
* Nigrostiatal pathways destroyed
* Imbalance of ACh, DA, GABA, Serotonin, etc
**Excess of ACh and a deficiency of DA
General HallMark Symptoms of Parkinson's
1. Rigidity
2. Resting Tremor
3. Bradykinesia
Motor Features of Parkinson's
1. Decreased dexterity
2. Difficulty speaking(dysarthria) and swallowing(dysphagia)
3. Quiet speaking(hypophonia), hypomimia(few facial expressions), micrographia(small writing)
4. Festinating Gait
Autonomic Features of Parkinson's
1. bladder disorder
2. constipation
3. fatigue
4. Skin problem(seborrhea)
5. Excessive salivating/drooling(sialorrhea)
6. orthostatic hypotension
Psychiatric Features of Parkinson's
1. anxiety
2. apathy
3. confusion
4. insomnia
5. depression
Diagnosis of Parkinson's
1. 2 of 3 hallmark features
2. response to pharmacotherapy
Initial Signs and Symptoms of Parkinson's
*Insidious onset
*usually sensory symptoms and tremor
*little impairment of activities
*no pharmacotherapy required
Advanced Signs and Symptoms of Parkinson's
*greater impairment of daily activities, quality of life
*psychiatric changes requiring additional pharmacotherapy
*hypomobility akinesia
Goals of Treatment of Parkinson's
1. Improve motor and non-motor function
2. maintain quality of life
3. avoid drug-induced complications
Non-Pharmacological Treatments of Parkinson's
1. Exercise
2. Nutrition
3. Education
4. Support Groups
5. Neurosurgery
Anticholinergics used to treat Parkinson's
1. Benztropine (Cogentin)
2. Trihexyphenidyl (Artane)
MAO-B Inhibitors used to treat Parkinson's
1. Selegiline (Eldepryl, Zelapar)
2. Rasagiline (Azilect)
COMT Inhibitors used to treat Parkinson's
1. Entacapone (Comtan)
2. Tolcapone (Tasmar)
Dopamine Agonists used to treat Parkinson's
1. Bromocriptine (Parlodel)
2. Ropinirole (Requip)
3. Pramipexole (Mirapex)
4. Apomorphine (Apokyn)
Other Medications used to treat Parkinson's
1. Carbidopa (Lodosyn)
2. Carbidopa/Levodopa (Sinemet, Parcopa)
3. Carbidopa/Levodopa/Entacapone (Stalevo)
4. Amantadine (Symmetrel)
Mechanism of Action of Anticholinergics for Parkinson's
overcomes the increased cholinergic activity
*balances ACh and DA*
Indication for Anticholinergics for Parkinsons
alone or as adjunct therapy
Clinical Pearls for Anticholinergics
1. most useful for tremor
2. sometimes useful for dystonia
3. little benefit for other clinical features
4. avoid use in elderly (over 65 years)
Possible MOA for Amantadine
increases DA release, inhibits DA reuptake, stimulates DA receptors or inhibits NMDA
Indication for use of Amantadine
Monotherapy or Symptomatic and adjunct treatment
ADRs for Amantadine
CV: orthostatic hypotension, peripheral edema
CNS: confusion, hallucinations, insomnia, agitation
GI: constipation, nausea, xerostomia
Derm: livedo reticularis
Dry Nose
Clinical Pearls for Amantadine
1. useful in early, mild disease
2. benefit for tremor, rigidity, bradykinesia
3. renally dosed
MOA of Levodopa
direct precursor to dopamine
1. penetrates CNS and is converted to dopamine by CENTRAL L-amino acid decarboxylase
2. can also be converted by PERIPHERAL L-amino acid decarboxylase and cannot enter CNS
MOA of Carbidopa
L-amino acid decarboxylase inhibitor - allows levodopa to escape conversion in the periphery
Indication for Levodopa/Carbidopa
Treatment in both early and late stages
*ultimately all patients will be on it
ADRs of Levodopa/Carbidopa
CV: arrhythmia(more common with levodopa alone), chest pain, orthostatic hypotension
CNS: anxiety, depression, abnormal dreams, hallucinations, confusion
GI: ab pain, diarrhea, constipation, nausea, vomit
Max dose of Carbidopa
200mg
Max dose of Levodopa
2000mg
Clinical Pearls for Levodopa/Carbidopa
1. most effective treatment
2. dyskinesias and other motor complications are common
3. akinesia improves rapidly & tremor/rigidity respond well. Balance/gain may not improve
Complications of DA therapy (levodopa/carbidopa)
1. Delayed-On or No-On
2. Wearing Off
3. On/Off
4. Dyskinesias
5. Freezing
6. Dystonias
7. Myclonus
8. Akathisia
"Delayed-On" or "No-On"
Signs: delayed or minimal response to previously effective dose

Treatment: give on empty stomach, chew or crush tab, switch to ODT, increase dose, add DA agonist
"Wearing off"
Signs: decreased duration of response; occurs at end of dose

Treatment: change to CR prep, increase frequency, add MAOB inhibitor or DA agonist or COMT inhibitor, long acting agents at night
"On/Off"
Signs: fluctuations from normal/good to poor movement

Treatment: add DA agonist, switch from IR to CR, add MAOB or COMT inhibitor
Dyskinesias
Signs: abnormal involuntary jerking of face, neck, arms, legs

Treatment: decrease dose, change to CR prep, add amantadine
"Freezing"
Signs: temporary, sudden, involuntary inability to move (usually lower extremities)

Treatment: increase dose, add DA agonist or MAOB inhibitor, physical therapy
Dystonias
Signs: sustained muscle contraction in early morning

Treatment: add DA agonist, dose CR at bedtime, baclofen
Myoclonus
Signs: repetitive jerking movements at night

Treatment: decrease nighttime dose, clonazepam
Akathisia
Signs: restless feeling

Treatment: add nighttime dopaminergic med
MOA of MAO-B inhibitor
selectively inhibits MAOa in the brain = inhibits DA degradation = enhanced dopaminergic activity
Indication of use for MAO-B inhibitor
1. adjunct therapy
2. initial monotherapy in early PD
Clinical Pearls with MAO-B Inhibitors
1. often used as initial monotherapy with mild symptoms
2. bioavailability is increased with ODT
ADRs of MAO-B Inhibitors
CNS: mood changes, insomnia, dizziness
GI: nausea, vomiting
Neuromuscular: dyskinesias
Warnings with MAO-B inhibitors
absolute contraindication with meperidine (Serotonin Syndrome)
MOA of COMT inhibitors
inhibit peripheral and central conversion of levodopa to dopamine by inhibiting catechol-o-methyltransferase enzyme
Indication for use of COMT Inhibitors
for combination therapy only, not first line
Warnings for COMT inhibitors (tolcapone)
fatal hepatotoxicity (reserved for last line)
ADRs of COMT inhibitors
CV: orthostatic hypotension, syncope
CNS: dizziness, fatigue, hallucination, anxiety
GI: nausea, vomit, diarrhea, constipation
Urinary: brown-orange urine color (COUNSEL)
Neuromuscular: dyskinesias, muscle cramps, stiffness
Clinical Pearls for COMT inhibitors
1. can allow a lower dose of levodopa
2. delayed onset of diarrhea (weeks to months later)
3. monitor LFTs at baseline then q2-4 week for 6 months
MOA of dopamine agonists
directly stimulate DA receptors
Indication of use for Dopamine agonists
initial monotherapy or adjunctive therapy to carbidopa/levodopa
ADRs of Dopamine Agonists
CV: orthostatic hypotension, edema, chest pain
CNS: somnolence, insomnia, dizziness, hallucinations
GI: nausea, constipation
Neuromuscular: dyskinesia, weakness
Dopamine agonist with highest incidence of ADRs
bromocriptine
Dopamine agonist that can be used as "rescue therapy" by subq injection
apomorphine
Clinical Pearls of Dopamine agonists
1. longer duration of action than levodopa & fewer motor complications
2. non-ergot agents have fewer ADRs
3. apomorphine requires pretreatment with trimethobenzamide(Tigan)
Essential Tremor
disorder of the nervous system that causes involuntary shaking movements that can affect any part of the body but usually the hands
Symptoms of Essential Tremor
1. small, rapid movements (5+ times per second)
2. "yes-yes" or "no-no" motion of head
3. shaking or quivering speech
Non Pharm Treatment of Essential Tremor
1. Relaxation techniques
2. avoid caffeine
3. use alcohol sparingly
4. obtain enough rest
2 classes of drugs used for treatment of Essential Tremor
1. Beta Blockers (Propranolol, Atenolol, sotalol, nadalol)
2. Primidone (anticonvulsant)
Clinical Pearl of Beta Blockers for Essential Tremor
1. most commonly used meds
Clinical Pearls for Primidone
Effective for limb tremor